Boyages S C, Bloot A M, Maberly G F, Eastman C J, Li M, Qian Q D, Liu D R, van der Gaag R D, Drexhage H A
Department of Medicine, Westmead Hospital, Sydney, Australia.
Clin Endocrinol (Oxf). 1989 Oct;31(4):453-65. doi: 10.1111/j.1365-2265.1989.tb01269.x.
The pathophysiology of endemic goitre caused by excessive iodine intake is not well defined. By interacting with the immune system, iodine excess may trigger the development of autoimmune thyroid disease such as lymphocytic Hashimoto's thyroiditis (LT). In an attempt to examine this further, we compared the presence of thyroid autoantibodies in 29 goitrous children, from an iodine excess area, and in 26 healthy children, from an iodine sufficient area, of north central China. Serum was tested for antimicrosomal (MAb), anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified IgG was tested for thyroid growth-stimulating activity (TGI) by two different methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid cell line (FRTL-5). We found no increased prevalence of LT in patients with endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ significantly between the two groups of children. Further, TBII were not present in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major autoantibodies found in children with goitres caused by iodine excess. In the CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy children were positive for TGI. Similar results were found in the MAA, and a good correlation between results of the CBA and MAA was found (P = 0.003). Maximal TGI activity in dose-response CBA showed a good relation with clinical goitre size (r = 0.63; P less than 0.05) indicating a possible pathophysiological role for these antibodies. We conclude that endemic iodine goitre is not associated with Hashimoto's lymphocytic thyroiditis. Nevertheless, autoimmune growth factors such as TGI may play a primary role in the pathogenesis of thyroid growth in this condition.
碘摄入过量所致地方性甲状腺肿的病理生理学机制尚未完全明确。通过与免疫系统相互作用，碘过量可能会引发自身免疫性甲状腺疾病的发展，如淋巴细胞性桥本甲状腺炎（LT）。为了进一步研究这一问题，我们比较了来自中国中部北部碘过量地区的29名甲状腺肿患儿和来自碘充足地区的26名健康儿童甲状腺自身抗体的情况。检测血清中的抗微粒体抗体（MAb）、抗甲状腺球蛋白抗体（TgAb）、第二胶体抗原抗体（CA2-Ab）和促甲状腺激素结合抑制性免疫球蛋白（TBII）。通过两种不同方法检测亲和层析纯化的IgG的甲状腺生长刺激活性（TGI）：一种是使用豚鼠甲状腺外植体的灵敏细胞化学生物测定法（CBA），另一种是采用连续大鼠甲状腺细胞系（FRTL-5）的有丝分裂抑制测定法（MAA）。我们发现地方性碘甲状腺肿患者中LT的患病率并未增加。两组儿童的MAb、TgAb和CA2-Ab水平无显著差异。此外，两组均未检测到TBII。甲状腺生长刺激免疫球蛋白（TGI）是碘过量所致甲状腺肿患儿中发现的主要自身抗体。在CBA中，20名甲状腺肿患儿中有12名（60%）TGI呈阳性，而12名健康儿童中无一例（0%，P<0.05）呈阳性。在MAA中也发现了类似结果，并且CBA和MAA的结果之间存在良好的相关性（P = 0.003）。剂量反应CBA中的最大TGI活性与临床甲状腺肿大小呈良好相关性（r = 0.63；P<0.05），表明这些抗体可能具有病理生理学作用。我们得出结论，地方性碘甲状腺肿与桥本淋巴细胞性甲状腺炎无关。然而，自身免疫性生长因子如TGI可能在这种情况下甲状腺生长的发病机制中起主要作用。
